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Researchers discover human gene, called stanniocalcin, which appears to be beneficial in control of the body's calcium level; key discovery in cancer treatment

NORMAN SWAN: Australian researchers have made an accidental discovery which could be extremely important for understanding and maybe even treating osteoporosis. It's a terrific example of how investment in basic research can turn up unexpected and often revolutionary findings.

Dr Andy Chang and a team led by Dr Roger Reddel of the Children's Medical Research Institute in Sydney have found that humans carry a gene for a fish hormone which seems to be very important in controlling the body's level of calcium - well, at least in fish.

The researchers were actually looking for cancer genes, genes which are switched on or off in the process of normal cells transforming themselves into malignant ones. The workers came across a gene which just happened to be switched off and, when they examined it further, they found that the gene held the genetic code for a hormone called stanniocalcin which the experts had hitherto thought only belonged to fish.

ROGER REDDEL: Yes, there were good reasons for believing that it only existed in fish. In fish, it's secreted by a particular endocrine gland which is found in no other species other than fish, and, in fish, it's involved in keeping calcium out. When the calcium levels rise too high for the fish, stanniocalcin stops uptake of calcium across the gills and across the bowel.

NORMAN SWAN: So either from the food that the fish is eating or from the calcium in the seawater, this stanniocalcin stops it getting overloaded with calcium?

ROGER REDDEL: That's right.

NORMAN SWAN: And was this a 'hot' area of fish research?

ROGER REDDEL: This was an area that received quite a lot of interest in the 1980s, and there have been groups in North America that have kept their interest in this.

NORMAN SWAN: Just in case it might have a human application?

ROGER REDDEL: I'm not sure what their motivation was but, certainly, a lot of this research has been funded by fisheries organisations.

NORMAN SWAN: Not wanting their fish to be clogged up with kidney stones or something like that! So you found this gene which was turned off, and it turns out to be - what, identical to the fish gene?

ROGER REDDEL: It's not quite identical, but it's extremely similar.

NORMAN SWAN: So it's likely or, in fact, almost certain, that human beings produce this calcium hormone which has hitherto only been thought to exist in fish?

ROGER REDDEL: That's right, it's extremely likely. And one difference that we've found is that we can't find any particular specialised endocrine gland whose sole role is to produce human stanniocalcin. It seems to be produced in a wide variety of tissues.

NORMAN SWAN: So it comes from everywhere. Do you think it has a role in calcium metabolism in humans?

ROGER REDDEL: Just based on its high degree of similarity to the fish hormone, I think it's extremely likely that it's got a role in calcium.

NORMAN SWAN: What could it be doing in cancer?

ROGER REDDEL: We don't know what it does in cancer. It may be acting as a growth factor for certain types of cells.

NORMAN SWAN: As I said earlier, cancer research is the main focus of Roger Reddel and his team's work. Coincidentally, at the weekend in the journal Science there were reports of key discoveries in an area which holds great promise for cancer treatment. It's a field which Roger Reddel 's team knows a lot about, and relates to a curious enzyme called telomerase. In many cancers, telomerase seems to turn up and be a critical part of the chain of events which leads to the uncontrolled multiplication of cells in cancer which is known as immortalisation. If you could knock out telomerase, perhaps you could pull the cancer cells back into line. Roger Reddel again.

ROGER REDDEL: That's correct. Our genetic material is packaged into structures called chromosomes, and at the end of each chromosome is a specialised structure called a telomere, which protects the end of the chromosome. In normal cells ....

NORMAN SWAN: What, it's like a button on the end of it that just protects it?

ROGER REDDEL: Yes. Some people have described it as being like the hard bit on a shoelace which protects it from fraying. Now, in normal cells in our bodies, a little bit gets lost from the end of the telomere every time the cell divides, and this apparently acts as a counting mechanism which ultimately limits the number of times our normal cells can divide - like a ticket, the end of which gets clipped off every time you ride on the bus. Now, it turns out that many cancer cells have learned how to evade this limit on proliferation that normal cells have.

NORMAN SWAN: Avoid the ticket inspector?

ROGER REDDEL: That's right. And they've done this by turning on an enzyme which is able to lengthen the telomeres. Telomerase is not found in normal cells.

NORMAN SWAN: So in other words, this enzyme is just turned on in cancer cells - an enzyme being a chemical which helps other reactions. And it stops this clock, this biological clock if you like, which stops division in the end and keeps the cell multiplying?

ROGER REDDEL: That's correct. This is one of the ways that cancer cells manage to evade the normal limits that are imposed on cells.

NORMAN SWAN: Presumably pharmaceutical companies are fascinated by this, because if you could turn off this enzyme you would stop the cells being immortal?

ROGER REDDEL: That's right. A recent study, just at the end of last year, found that this enzyme was present in approximately 90 per cent of all tumours.

NORMAN SWAN: So it really is a fundamental part of the cancer process?

ROGER REDDEL: It seems to be an extremely important part and a common part.

NORMAN SWAN: And how likely is it that somebody could find a way of blocking this telomerase?

ROGER REDDEL: I think it's only a matter of time before inhibitors can be found.

NORMAN SWAN: Dr Roger Reddel is head of the Cancer Research Group at the Children's Medical Research Institute in Sydney.